Baroreflex dysfunction in diabetes mellitus. I. Selective impairment of parasympathetic control of heart rate

1994 ◽  
Vol 266 (1) ◽  
pp. H235-H243 ◽  
Author(s):  
T. S. McDowell ◽  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Diabetes Mellitus ◽  
Heart Rate ◽  
Blood Glucose ◽  
Arterial Pressure ◽  
Adrenergic Blockade ◽  
Baroreflex Control ◽  
Parasympathetic Control ◽  
Diabetic Rabbits ◽  
Selective Impairment ◽  
Increased Pressure

The purpose of this study was to determine the effect of diabetes mellitus on baroreflex control of heart rate. Diabetes (blood glucose = 378 +/- 21 mg/dl) was induced in rabbits by alloxan (n = 9). Alloxan-treated rabbits that remained normoglycemic (n = 9) and rabbits given saline instead of alloxan (n = 5) served as controls. Baroreflex control of heart rate was evaluated in conscious rabbits by measuring changes in heart rate during phenylephrine-induced increases and nitroglycerin-induced decreases in arterial pressure. In diabetic rabbits, the gain of the baroreflex-mediated bradycardia in response to increased pressure decreased significantly from -1.8 +/- 0.3 beats.min-1 x mmHg-1 before alloxan (n = 9) to -0.9 +/- 0.1 and -0.9 +/- 0.3 beats.min-1 x mmHg-1 after 12 and 24 wk of diabetes, respectively (n = 8; P < 0.05). There was no significant change in baroreflex gain in either alloxan-treated or saline-treated normoglycemic rabbits. Baroreflex-mediated bradycardia was not influenced significantly after beta-adrenergic blockade with propranolol (1 mg/kg) and was still impaired in diabetic vs. control rabbits after propranolol. The gain of the baroreflex-mediated tachycardia in response to decreased pressure was not altered in any of the three groups. Propranolol significantly decreased but did not abolish baroreflex-mediated tachycardia. Neither the vagal nor the sympathetic component of the tachycardia was altered significantly by diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Compensatory recovery of parasympathetic control of heart rate after unilateral vagotomy in rabbits

1992 ◽  
Vol 262 (4) ◽  
pp. H1122-H1127 ◽  
Author(s):  
D. D. Lund ◽  
G. A. Davey ◽  
A. R. Subieta ◽  
B. J. Pardini
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Vagal Stimulation ◽  
Acetylcholinesterase Inhibition ◽  
Baroreflex Control ◽  
Recovery Mechanism ◽  
Vagal Innervation ◽  
Increased Sensitivity ◽  
Parasympathetic Control

Compensatory recovery by the intact vagal innervation after unilateral vagotomy was investigated by measuring parasympathetic-mediated control of heart rate in beta-adrenergic-blocked rabbits. Direct contralateral vagal nerve stimulation produced greater bradycardia in anesthetized rabbits with chronic vagotomy compared with acutely vagotomized controls. Vagal stimulation during acetylcholinesterase inhibition by physostigmine and direct neuroeffector stimulation by methacholine indicated that a change in metabolism of the neurotransmitter or an increased sensitivity of the tissue to acetylcholine were not responsible for augmentation of vagal responses. Baroreflex control of heart rate in response to an increase in arterial pressure was also tested in urethan-anesthetized rabbits. There was a significant reduction in the prolongation of the R-R interval during baroreflex activation acutely after midcervical vagotomy. These values were subsequently above control levels in rabbits 28 days after vagotomy. In conscious rabbits, the decrease in baroreflex control of heart rate progressively recovered to control levels within 6 days. These results suggest that the recovery mechanism after unilateral vagotomy may be related to peripheral and central compensatory changes in the intact contralateral vagus nerve.

Anti-Diabetic Effect of a Flavonoid and Sitosterol - Rich Aqueous Extract ofPleurotus tuberregiumSclerotia in Alloxan-Induced Diabetic Rabbits

2019 ◽  
Vol 19 (8) ◽  
pp. 1148-1156 ◽  
Author(s):  
Ifeanacho Mercy Onuekwuzu ◽  
Ikewuchi Catherine Chidinma ◽  
Ikewuchi Jude Chigozie
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Aqueous Extract ◽  
Risk Index ◽  
Fasting Blood Glucose ◽  
Hdl Cholesterol ◽  
The Body ◽  
Atherogenic Index ◽  
Atherogenic Indices ◽  
Diabetic Rabbits

Objective:Traditionally prepared infusions and decoctions are commonly used in the management of diabetes mellitus, in southern Nigeria; one of such is the aqueous extract of the sclerotia of Pleurotus tuberregium (“usu” milk). In this study, the effects of the extract on the body weights, tissue/ organ weights, fasting blood glucose, blood/plasma lipid profiles and atherogenic indices were investigated in normal and alloxan-induced diabetic rabbits.Methods:Diabetes mellitus was induced by the injection of alloxan (120 mg/kg body weight) via the marginal ear vein. The extract was administered orally at 100, 200 and 300 mg/kg to normal and diabetic rabbits; while metformin was administered at 50 mg/kg. The crude extract was analyzed by gas chromatography, coupled to flame ionization detector.Results:Thirty-one known flavonoids were detected, consisting mainly of isoquercetin (28.5%), luteolin (24.3%), quercetin (18.8%) and kaempferol (11.3%). Sitosterol (82.0%) and stigmasterol (12.5%) were the most abundant of the seven phytosterols detected. Compared to the diabetic control, the treatment significantly (p<0.05) lowered the weights of the kidney and liver, as well as the levels of blood glucose and triglyceride, plasma VLDL, LDL and non-HDL cholesterol, atherogenic index of plasma, cardiac risk ratio, atherogenic coefficient and Castelli’s risk index II. It, however, significantly (p<0.05) increased plasma HDL cholesterol, without significantly affecting blood total cholesterol levels.Conclusion:This study showed that the extract was hypoglycemic, and improved lipid profile and atherogenic indices, thus highlighting its cardioprotective potential, thereby supporting its use in the management of diabetes mellitus.

scholarly journals Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Afferents ◽  
Baroreflex Control ◽  
Group Iii ◽  
Carotid Baroreflex

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Heart Rate Response ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Arterial Pressure ◽  
Normal Subjects ◽  
Vagus Nerves ◽  
Baroreflex Control

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

Thyroid status influences baroreflex function and autonomic contributions to arterial pressure and heart rate

2001 ◽  
Vol 280 (5) ◽  
pp. H2061-H2068 ◽  
Author(s):  
C. Michael Foley ◽  
Richard M. McAllister ◽  
Eileen M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Arterial Baroreflex ◽  
Thyroid Status ◽  
Baroreflex Control ◽  
Baroreflex Function ◽  
Resting Blood Pressure ◽  
Sympathetic Influence

The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.

Impaired baroreflex control of vascular resistance in prehypertensive Dahl S rats

1983 ◽  
Vol 245 (2) ◽  
pp. H210-H217 ◽  
Author(s):  
F. J. Gordon ◽  
A. L. Mark
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Strain Difference ◽  
Sympathetic Innervation ◽  
Baroreflex Control ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Elevated Arterial Pressure

The purpose of this study was to examine baroreflex control of vascular resistance and heart rate in prehypertensive Dahl salt-sensitive (DS) and salt-resistant (DR) rats. Urethan-anesthetized normotensive DS rats demonstrated significantly impaired baroreflex control of both hindlimb vascular resistance and heart rate. This impairment was not secondary to elevated arterial pressure since blood pressure did not differ between DR and DS rats fed a low sodium diet. Vascular baroreflex responses were shown to depend on the integrity of efferent sympathetic innervation and to be mediated by the sinoaortic afferent arterial baroreceptors. No strain difference was observed for hindlimb vasodilation produced by papaverine or graded doses of nitroprusside, indicating that differences in resistance vessel vasodilator capacity or responsiveness could not account for differences in baroreflex responses. Since impaired baroreflex control was evident in DS rats prior to any elevation in arterial pressure, this abnormality may contribute to the DS rat's genetic propensity to develop hypertension.

Hemodynamic effects of vasopressin compared with angiotensin II in conscious rats

1987 ◽  
Vol 252 (3) ◽  
pp. H628-H637 ◽  
Author(s):  
J. W. Osborn ◽  
M. M. Skelton ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Fold Increase ◽  
Adrenergic Blockade ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Potent Vasoconstrictor

The mechanisms whereby arginine vasopressin influences hemodynamic and autonomic function were investigated in conscious rats. In normal rats, 60-min intravenous infusions produced dose-related increases of arterial pressure and total peripheral resistance with marked decreases of both heart rate and cardiac output. Cholinergic blockade with methscopolamine attenuated the bradycardia at higher doses of vasopressin, whereby the fall of cardiac output was not affected. beta-Adrenergic blockade with atenolol attenuated the fall of heart rate seen with lower doses of vasopressin but did not prevent the fall of cardiac output. Ganglionic blockade with methscopolamine and hexamethonium resulted in nearly a 60-fold enhancement of vasopressin pressor sensitivity. This was related to a greater rise of peripheral resistance, since the fall of cardiac output was not altered compared with normal rats. Hemodynamic responses to angiotensin II were determined in other groups of conscious, normal rats and rats with ganglionic blockade. Peripheral resistance increased in the normal rats, whereas the related decreases in cardiac output and heart rate were only 30% of the responses seen with equipressor doses of vasopressin. Ganglionic blockade increased pressor activity only two- to eightfold compared with the 60-fold increase observed with vasopressin. We conclude that vasopressin is a more potent vasoconstrictor than angiotensin II, decreases cardiac output independent of neural mechanisms, and results in withdrawal of sympathetic vascular tone to buffer rises of arterial pressure.

scholarly journals Chronic baroreflex activation restores spontaneous baroreflex control and variability of heart rate in obesity-induced hypertension

2013 ◽  
Vol 305 (7) ◽  
pp. H1080-H1088 ◽  
Author(s):  
Radu Iliescu ◽  
Ionut Tudorancea ◽  
Eric D. Irwin ◽  
Thomas E. Lohmeier
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Arterial Pressure ◽  
Cardiac Arrhythmias ◽  
High Fat Diet ◽  
Renal Denervation ◽  
Gradual Increase ◽  
High Fat ◽  
Baroreflex Control ◽  
Cardiovascular Dynamic

The sensitivity of baroreflex control of heart rate is depressed in subjects with obesity hypertension, which increases the risk for cardiac arrhythmias. The mechanisms are not fully known, and there are no therapies to improve this dysfunction. To determine the cardiovascular dynamic effects of progressive increases in body weight leading to obesity and hypertension in dogs fed a high-fat diet, 24-h continuous recordings of spontaneous fluctuations in blood pressure and heart rate were analyzed in the time and frequency domains. Furthermore, we investigated whether autonomic mechanisms stimulated by chronic baroreflex activation and renal denervation—current therapies in patients with resistant hypertension, who are commonly obese—restore cardiovascular dynamic control. Increases in body weight to ∼150% of control led to a gradual increase in mean arterial pressure to 17 ± 3 mmHg above control (100 ± 2 mmHg) after 4 wk on the high-fat diet. In contrast to the gradual increase in arterial pressure, tachycardia, attenuated chronotropic baroreflex responses, and reduced heart rate variability were manifest within 1–4 days on high-fat intake, reaching 130 ± 4 beats per minute (bpm) (control = 86 ± 3 bpm) and ∼45% and <20%, respectively, of control levels. Subsequently, both baroreflex activation and renal denervation abolished the hypertension. However, only baroreflex activation effectively attenuated the tachycardia and restored cardiac baroreflex sensitivity and heart rate variability. These findings suggest that baroreflex activation therapy may reduce the risk factors for cardiac arrhythmias as well as lower arterial pressure.

Disrupted circadian rhythms of body temperature, heart rate and fasting blood glucose in prediabetes and type 2 diabetes mellitus

2017 ◽  
Vol 34 (8) ◽  
pp. 1136-1148 ◽  
Author(s):  
D. G. Gubin ◽  
A. A. Nelaeva ◽  
A. E. Uzhakova ◽  
Y. V. Hasanova ◽  
G. Cornelissen ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Heart Rate ◽  
Type 2 Diabetes Mellitus ◽  
Blood Glucose ◽  
Body Temperature ◽  
Circadian Rhythms ◽  
Fasting Blood Glucose
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